Membranotropic activity of taurine derivatives

2020 ◽  
Author(s):  
Petr D. Shabanov ◽  
Ludmila K. Khnychenko
Keyword(s):  
Sulfonic Acid ◽  
Lymnaea Stagnalis ◽  
Calcium Influx ◽  
Ionic Currents ◽  
Isolated Neurons ◽  
Excitable Cells ◽  
Potassium Efflux ◽  
Low Concentrations ◽  
High Concentrations ◽  
Derivatives Of

The aim of the work. To evaluate the effect of n-phenylalkyl derivatives of taurine on changes in transmembrane ion currents of potential-controlled ion channels of isolated neurons. Materials and methods. The method of intracellular dialysis and fixation of membrane potential on isolated neurons of the great pond truncatula (Lymnaea stagnalis) and hornbill (Planorbarius corneus) was used. The n-phenylalkyl derivatives of taurine (1-phenyl-2-isopropylaminoethanesulfonic acid; benzylaminoethane sulfonic acid isopropylamide; phenethylaminoethane sulfonic acid isopropylamide) or the comparison drug taurine was dissolved in external solutions and studied at concentrations of 1, 10, 100 and 1000 M. Results. The results demonstrate that n-phenilalkyl derivatives of taurine in low concentrations (1; 10 M) have a modulating effect on electrically excitable cells, and in high concentrations (100; 1000 M) reduce the sodium-calcium influx and potassium efflux ionic currents, have a channel blocking effect. Conclusion. N-phenylalkyl derivatives of taurine reduces the excitability of cells contribute to the suppression of synaptic potentials, ion gradients of the cells.

scholarly journals Modulation of electrical activity and ionic currents of isolated neurons by orexin A

2013 ◽  
Vol 11 (4) ◽  
pp. 54-60
Author(s):  
Petr Dmitriyevich Shabanov ◽  
Anatoliy Ivanovich Vislobokov
Keyword(s):  
Membrane Potential ◽  
Lymnaea Stagnalis ◽  
Ionic Currents ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Isolated Neurons ◽  
Orexin A ◽  
High Concentrations ◽  
Kinetics Of ◽  
Dose Dependent

The changes in intracellular potential of resting (PR) and potential of action (PA) of the identified neurons of pedal and visceral ganglia of the CNS mollusk Planorbarius corneus registered by means of intracellular electrodes, and ionic currents of isolated neurons under fixed potential after administration of orexin A in concentrations 1, 10, 100 and 1000 µg/ml were studied by the method of fixation of membrane potential in isolated neurons of the Lymnaea stagnalis mollusk. Dibazol in concentrations of 1 and 10 µM effected slightly on the ionic currents. High concentrations of dibazol (100 and 1000 µM) inhibited all currents in dose dependent manner with maximal effect on potassium currents amplitude. ЕС50 were 7.4 мМ for INa, 4.0 мМ for ICa, 83.9 µM for IKs,1 (one group of neurons) and 2.9 мМ for IKs,2 (the another group of neurons). The voltage-amper membrane characteristics shift was not registered, but the kinetics of currents development was changed. Dibazol was more effective in inhibition of ionic currents compared to its structural analogs.

scholarly journals THE MOLLUSC IONIC CURRENTS CHANGES AFTER ADMINISTRATION OF N-PHENYLALKYL DERIVATIVES OF TAURINE

2012 ◽  
Vol 10 (4) ◽  
pp. 67-72
Author(s):  
Anatoliy Ivanovich Vislobokov ◽  
Lyudmila Konstantinovna Khnychenko ◽  
Yuriy Dmitriyevich Ignatov ◽  
Nikolay Sergeyevich Sapronov ◽  
Petr Dmitriyevich Shabanov
Keyword(s):  
Lymnaea Stagnalis ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Dependent Manner ◽  
Isolated Neurons ◽  
Sodium Potassium ◽  
Fixed Membrane ◽  
Kinetics Of ◽  
Dose Dependent ◽  
Derivatives Of

The transmembrane sodium, potassium and calcium ionic currents were studied after extracellular administration of N-phenylalkyl derivatives of taurine in concentrations 1, 10, 100 and 1000 mM. The method of intracellular dialysis with fixed membrane potential was used in model of isolated neurons of the mollusks Lymnaea stagnalis and Planorbarius corneus. The solutions containing 1 and 10 mM of the compounds studied did not change ionic channels activity in isolated neurons. Concentrations 100 and mM depressed reversibly all currents in the dose-dependent manner: taurine < TAU-02 < TAY-15 < TAU-60. The voltage-amplitude membrane characteristics as well as kinetics of the currents did not change.

scholarly journals Effect of dibazol and its new derivatives on the mollusk ionic channels

2013 ◽  
Vol 11 (3) ◽  
pp. 26-32
Author(s):  
Anatoliy Ivanovich Vislobokov ◽  
Leonid Vitalyevich Myznikov ◽  
Aleksandr Aleksandrovich Tarasenko ◽  
Petr Dmitriyevich Shabanov
Keyword(s):  
Lymnaea Stagnalis ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Isolated Neurons ◽  
High Concentrations ◽  
Kinetics Of ◽  
Dose Dependent ◽  
Sodium And Potassium

The changes in transmembrane calcium, sodium and potassium ionic currents after extracellular administration of dibazol (2-(phenylmethyl)-1H-benzimidazol hydrochloride) and its two new derivatives in concentrations of 1, 10, 100 and 1000 µM were studied by the method of intracellular dialysis and fixation of membrane potential in isolated neurons of the Lymnaea stagnalis mollusk. Dibazol in concentrations of 1 and 10 µM effected slightly on the ionic currents. High concentrations of dibazol (100 and 1000 µM) inhibited all currents in dose dependent manner with maximal effect on potassium currents amplitude. ЕС50 were 7.4 мМ for INa, 4.0 мМ for ICa, 83.9 µM for IKs,1 (one group of neurons) and 2.9 мМ for IKs,2 (the another group of neurons). The voltage-amper membrane characteristics shift was not registered, but the kinetics of currents development was changed. Dibazol was more effective in inhibition of ionic currents compared to its structural analogs.

INCORPORATION OF INORGANIC P32INTO PHOSPHOLIPIDS OF BRAIN SLICES: EFFECT OF CERTAIN TRANQUILLIZING DRUGS

1963 ◽  
Vol 41 (1) ◽  
pp. 1155-1162 ◽  
Author(s):  
W. L. Magee ◽  
R. J. Rossiter
Keyword(s):  
Methylene Blue ◽  
Guinea Pig ◽  
Aerobic Glycolysis ◽  
Brain Slices ◽  
Inorganic P ◽  
Pig Brain ◽  
Low Concentrations ◽  
High Concentrations ◽  
Derivatives Of ◽  
Guinea Pig Brain

Promazine, promethazine, tetrameprazine, and WY 1172, four tranquillizing drugs that are derivatives of phenothiazine, resembled chlorpromazine in that when they were added in a concentration of 0.1 mM to slices of guinea pig brain respiring in a suitable medium they stimulated the incorporation of inorganic P32into the phospholipids of the slices. With one of the drugs, promethazine, this concentration of 0.1 mM was found to cause no significant increase in respiration, in aerobic glycolysis, or in the concentration of phosphocreatine. In higher concentrations (1.0 mM), all of the compounds inhibited the labelling of phospholipid. Promethazine caused a reduction in respiration and in the concentration of phosphocreatine, accompanied by an increase in aerobic glycolysis. Methylene blue, a derivative of phenothiazine with no reported tranquillizing properties, did not stimulate the labelling of phospholipid in brain slices. Azacyclonol, pipradrol, and mepazine, drugs that are derivatives of piperidine, also stimulated phospholipid labelling in low concentrations and inhibited the labelling at higher concentrations. Piperidine and benzhydrol, the two components from which azacyclonol is derived, did not stimulate phospholipid labelling at the concentration which was most effective for azacyclonol. Low concentrations of benzhydrol, however, caused a slight stimulation. Meprobamate and phenaglycodol, two other compounds with reputed tranquillizing action, had either little or no effect. Most of the substances tested inhibited phospholipid labelling when they were added in sufficiently high concentrations.

2,3-Butanediol in plasma from an alcoholic mistakenly identified as ethylene glycol by gas-chromatographic analysis

1991 ◽  
Vol 37 (8) ◽  
pp. 1453-1455 ◽  
Author(s):  
A W Jones ◽  
L Nilsson ◽  
S A Gladh ◽  
K Karlsson ◽  
J Beck-Friis
Keyword(s):  
Gas Chromatography ◽  
Ethylene Glycol ◽  
Chromatographic Analysis ◽  
Enzymatic Production ◽  
Low Concentrations ◽  
Elimination Half ◽  
Ethylene Glycol Poisoning ◽  
Incorrect Diagnosis ◽  
High Concentrations ◽  
Derivatives Of

Abstract 2,3-Butanediol was mistakenly identified as ethylene glycol in plasma specimens from two alcoholic patients. The cyclic phenylboronate ester derivatives of 2,3-butanediol and ethylene glycol had the same retention time when OV-17 was used as the stationary phase for gas chromatography. This led to incorrect diagnosis of ethylene glycol poisoning and unnecessary invasive therapy. Plasma from two chronic alcoholics contained 2,3-butanediol at 3.5 and 3.4 mmol/L. The elimination half-life of 2,3-butanediol was 3.9 days when ethanol was administered during therapy for suspected ethylene glycol poisoning. Low concentrations of 2,3-butanediol might be present in blood of chronic alcoholics as a result of a novel pathway of intermediary metabolism associated with some forms of alcoholism. However, a more likely explanation for fairly high concentrations of 2,3-butanediol is enzymatic production from 2-butanone. This ketone occurs in denatured alcohol preparations often consumed by alcoholics in Sweden.

Pharmacology of the myogenic heart of the pond snail Lymnaea stagnalis

1990 ◽  
Vol 63 (6) ◽  
pp. 1413-1425 ◽  
Author(s):  
K. J. Buckett ◽  
G. J. Dockray ◽  
N. N. Osborne ◽  
P. R. Benjamin
Keyword(s):  
Lymnaea Stagnalis ◽  
Isolated Heart ◽  
Rapid Onset ◽  
Heart Tissue ◽  
Pond Snail ◽  
Low Concentrations ◽  
Other Substances ◽  
Heart Preparation ◽  
High Concentrations ◽  
Alpha Bungarotoxin

1. We have used pharmacologic, immunologic, and biochemical techniques to examine the role of neurochemicals in modulating the myogenic heart of the snail, Lymnaea. 2. 5-HT [high-pressure liquid chromatography (HPLC) and immunocytochemistry], dopamine (HPLC), FMRFamide-related peptides (radioimmunoassay and immunocytochemistry) and substance P-related peptides (immunocytochemistry) were shown to be localized within heart tissue. 3. The pharmacologic actions of these substances on the auricle from an isolated heart preparation were examined together with other putative modulators, acetylcholine (ACh), small cardioactive peptides A and B (SCPA and SCPB), [Arg]8vasotocin (AVT), and Lymnaea native FMRFamide-related peptides [Phe-Met-Arg-Phe-NH2 (FMRFamide), Ser-Asp-Pro-Phe-Leu-Arg-Phe-NH2 (SDPFLRFamide) and Gly-Asp-Pro-Phe-Leu-Arg-Phe-NH2 (GDPFLRFamide)]. 4. The response to each substance could be distinguished by different effect on beat rate, amplitude, and diastolic tonus, as well as by the duration of responses to standard 1-min applications. ACh was inhibitory at low concentrations (threshold less than 10(-10) M) but excitatory at high concentrations (10(-6) M). AVT was alone in producing no dose-dependent response. At high concentrations (10(-4) M), AVT caused a massive tonic contraction and cessation of auricle beat. All other substances examined were excitatory. 5. Antagonists to 5-HT (cinanserin), dopamine (ergonovine), and ACh (alpha-bungarotoxin) were identified. 6. ACh, 5-HT, dopamine, and FMRFamide-related peptides all acted on the auricle at low concentrations, and the rapid onset and short duration of their excitatory effects (ACh inhibitory at low concentrations) suggested that they may have roles as neurotransmitters. SCPA and SCPB were also potent (threshold less than 10(-10) M) but produced long-duration responses suggesting a modulatory or hormonal role.

scholarly journals Changes in neuronal ionic currents after extracellular and intracellular administration of afobazol and bupivacaine

2014 ◽  
Vol 12 (3) ◽  
pp. 50-55 ◽  
Author(s):  
Anatoliy Ivanovich Vislobokov ◽  
Konstantin Nikolayevich Melnikov ◽  
Petr Dmitriyevich Shabanov
Keyword(s):  
Local Anesthetic ◽  
Lymnaea Stagnalis ◽  
External Surface ◽  
Ionic Currents ◽  
Neuronal Membrane ◽  
Isolated Neurons ◽  
Inhibition Effect ◽  
Planorbarius Corneus ◽  
Pharmacological Targets

The action of anxiolytic afobazol (2-mercaptobenzimidazolum derivative) in concentration 1 mM and local anesthetic bupivacaine in concentrations 0,5-1 mM on ionic currents of isolated neurons of Lymnaea stagnalis and Planorbarius corneus was studied. The method of intracellular dialysis was used in the experiment. Afobazol and bupivacaine after intracellular administration was shown not to possess their inhibition effect of ionic currents, typical for extracellular administration of drugs. It is suggested that pharmacological targets or bindind sits for these drugs are located on external surface of neuronal membrane.

INCORPORATION OF INORGANIC P32INTO PHOSPHOLIPIDS OF BRAIN SLICES: EFFECT OF CERTAIN TRANQUILLIZING DRUGS

1963 ◽  
Vol 41 (5) ◽  
pp. 1155-1162 ◽  
Author(s):  
W. L. Magee ◽  
R. J. Rossiter
Keyword(s):  
Methylene Blue ◽  
Guinea Pig ◽  
Aerobic Glycolysis ◽  
Brain Slices ◽  
Inorganic P ◽  
Pig Brain ◽  
Low Concentrations ◽  
High Concentrations ◽  
Derivatives Of ◽  
Guinea Pig Brain

Promazine, promethazine, tetrameprazine, and WY 1172, four tranquillizing drugs that are derivatives of phenothiazine, resembled chlorpromazine in that when they were added in a concentration of 0.1 mM to slices of guinea pig brain respiring in a suitable medium they stimulated the incorporation of inorganic P32into the phospholipids of the slices. With one of the drugs, promethazine, this concentration of 0.1 mM was found to cause no significant increase in respiration, in aerobic glycolysis, or in the concentration of phosphocreatine. In higher concentrations (1.0 mM), all of the compounds inhibited the labelling of phospholipid. Promethazine caused a reduction in respiration and in the concentration of phosphocreatine, accompanied by an increase in aerobic glycolysis. Methylene blue, a derivative of phenothiazine with no reported tranquillizing properties, did not stimulate the labelling of phospholipid in brain slices. Azacyclonol, pipradrol, and mepazine, drugs that are derivatives of piperidine, also stimulated phospholipid labelling in low concentrations and inhibited the labelling at higher concentrations. Piperidine and benzhydrol, the two components from which azacyclonol is derived, did not stimulate phospholipid labelling at the concentration which was most effective for azacyclonol. Low concentrations of benzhydrol, however, caused a slight stimulation. Meprobamate and phenaglycodol, two other compounds with reputed tranquillizing action, had either little or no effect. Most of the substances tested inhibited phospholipid labelling when they were added in sufficiently high concentrations.

Role of calcium fluxes in the action of glucagon on glucose metabolism in rat hepatocytes

1993 ◽  
Vol 265 (1) ◽  
pp. G35-G42 ◽  
Author(s):  
T. Mine ◽  
I. Kojima ◽  
E. Ogata
Keyword(s):  
Glucose Metabolism ◽  
Calcium Influx ◽  
Rat Hepatocytes ◽  
Extracellular Calcium ◽  
Free Calcium ◽  
Isolated Rat Hepatocytes ◽  
Calcium Fluxes ◽  
Low Concentrations ◽  
High Concentrations

The aim of the present study was to assess the role of calcium fluxes in the action of glucagon on glycogenolysis and gluconeogenesis in isolated rat hepatocytes. Calcium influx was blocked by two ways: by use of the compound tetramethrin and by reduction of extracellular calcium to 1 microM. The minimal concentration of tetramethrin that inhibited glucagon-mediated calcium entry was 7.5 x 10(-7) M. In the presence of 7.5 x 10(-7) M tetramethrin, glucagon-induced glycogenolysis was markedly attenuated when glucagon concentration was 10(-9) M or higher. In contrast, tetramethrin had no effect on glucogenolysis evoked by lower concentrations of glucagon. Similarly, tetramethrin greatly reduced gluconeogenesis induced by high concentrations of glucagon without affecting the effect of low concentrations of glucagon. The same results were obtained in the presence of 1 microM extracellular calcium. To abolish glucagon-induced elevation of cytoplasmic free calcium concentration, we heavily loaded quin2 into hepatocytes. In these cells, glycogenolysis evoked by low concentrations of glucagon was completely abolished. Glycogenolysis caused by high concentrations of glucagon was markedly inhibited. These results indicate that glucagon action on hepatic glucose metabolism is mediated by two different mechanisms, which depend on concentrations of glucagon.

Neutrophil Elastase Potentiates Cathepsin G-lnduced Platelet Activation

1992 ◽  
Vol 68 (05) ◽  
pp. 570-576 ◽  
Author(s):  
Mary A Selak
Keyword(s):  
Neutrophil Elastase ◽  
Cell Activation ◽  
Thromboxane A2 ◽  
Creatine Phosphate ◽  
Dense Granule ◽  
Cathepsin G ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Low Concentrations ◽  
High Concentrations

SummaryWe have previously demonstrated that human neutrophil cathepsin G is a strong platelet agonist that binds to a specific receptor. This work describes the effect of neutrophil elastase on cathepsin G-induced platelet responses. While platelets were not activated by high concentrations of neutrophil elastase by itself, elastase enhanced aggregation, secretion and calcium mobilization induced by low concentrations of cathepsin G. Platelet aggregation and secretion were potentiated in a concentration-dependent manner by neutrophil elastase with maximal responses observable at 200 nM. Enhancement was observed when elastase was preincubated with platelets for time intervals of 10–60 s prior to addition of a low concentration of cathepsin G and required catalytically-active elastase since phenylmethanesulphonyl fluoride-inhibited enzyme failed to potentiate cell activation. Neutrophil elastase potentiation of platelet responses induced by low concentrations of cathepsin G was markedly inhibited by creatine phosphate/creatine phosphokinase and/or indomethacin, indicating that the synergism between elastase and cathepsin G required the participation of ADP and thromboxane A2. On the other hand, platelet responses were not attenuated by the PAF antagonist BN 52021, signifying that PAF-acether did not play a role in elastase potentiation. At higher concentrations porcine pancreatic elastase exhibits similar effects to neutrophil elastase, demonstrating that the effect of elastase was not unique to the neutrophil protease. While neutrophil elastase failed to alter the ability of cathepsin G to hydrolyze a synthetic chromogenic substrate, preincubation of platelets with elastase increased the apparent affinity of cathepsin G binding to platelets. In contrast to their effect on cathepsin G-induced platelet responses, neither neutrophil nor pancreatic elasatse potentiated aggregation or dense granule release initiated by ADP, PAF-acether, arachidonic acid or U46619, a thromboxane A2 mimetic. Moreover, unlike its effect on cathepsin G, neutrophil elastase inhibited thrombin-induced responses. The current observations demonstrate that elastase can potentiate platelet responses mediated by low concentrations of cathepsin G, suggesting that both enzymes may function synergistically to activate platelets under conditions where neutrophil degranulation occurs.

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